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Kouichi Ito, PhD

Associate Professor

Phone:(732) 235-5482
Fax: 732-235-4773
Email: itoko@rwjms.rutgers.edu

Biography

Dr. Kouichi Ito is currently an Associate Professor in the Department of Neurology at Rutgers-Robert Wood Johnson Medical School. He received training in molecular immunology as a visiting scientist at MIT (1986-1990) and earned his PhD in Immunology from The Jikei University School of Medicine in Tokyo, Japan (1991). Prior to assuming his position at Rutgers-RWJMS, he served as a Laboratory Head within the Department of Immunology at Hoffmann-La Roche (Nutley, NJ) and studied the effects of Human Leukocyte Antigen (HLA) on the development of autoimmune diseases including Multiple Sclerosis (1992-1998). He also served as the Acting Chief of the Neurological Disease Section in the Neuroimmunology Branch at NIH/NINDS and studied the mechanism of encephalitogenic T cell development using humanized animal models of Multiple Sclerosis (1998-2003). His lab currently focuses on understanding the mechanisms of inflammation-associated neurodegeneration and the linkage between the gut immune system and neurological disorders. Research Interests: Development of new treatments for Multiple Sclerosis. Mechanisms of immune-mediated neuroinflammation and demyelination/axonal loss. A linkage between the gut immunity and neurological disorders.

Recent publication

  1. Yadav SK, Mindur JE, Ito K, Dhib-Jalbut S. Advances in the immunopathogenesis of multiple sclerosis. Curr Opin Neurol. 2015 Apr 17.
  2. Mindur E.J., Ito N., l Dhib-Jalbut S. and Ito K. Early treatment with anti-VLA-4 mAb can prevent the infiltration and/or development of pathogenic CD11b+CD4+ T cells in the CNS during progressive EAE. PLOS ONE 2014 Jun 4;9 (6):e99068.
  3. Boppana S., Mindur J.E., Balashov K.E., Dhib-Jalbut S. and Ito K. Comparison of IFN-β inducible gene expression in primary-progressive and relapsing-remitting multiple sclerosis. J. Neuroimmunology 265:68-74 (2013)
  4. Dhib-Jalbut S., Valenzuela R, Ito K, Kaufman M, Picone MA, Buyske S. HLA DR and DQ alleles and haplotypes associated with clinical response to glatiramer acetate in multiple sclerosis. Multiple Sclerosis and Related Disorders. 2; 340–348 (2013)
  5. Huang H, Ito K*, Dangond F, Dhib-Jalbut S*. Effect of interferon beta-1a on B7.1 and B7.2 B-cell expression and its impact on T-cell proliferation. J Neuroimmunol., 258:27-30 (2013) * contributed equally
  6. Dhib-Jalbut S, Sumandeep S, Valenzuela R, Ito K, Patel P, Rametta M. immune response during interferon beta-1b treatment in patients with multiple sclerosis who experienced relapses and those who were relapse-free in the START study. J Neuroimmunol., 254:131-40 (2013)
  7. Quandt J.A., Huh J., Baig M., Yao K., Ito N., Bryant M., Kawamura K., Pinilla C., McFarland H.F., Martin R., Ito K. Myelin Basic Protein-Specific TCR/ HLA-DRB5*01:01 Transgenic Mice Support the Etiologic Role of DRB5*01:01 in Multiple Sclerosis. J. Immunology; 89(6):2897-908 (2012)
  8. Boppana S, Huang H, Ito K, Dhib-Jalbut S. Immunologic aspects of multiple sclerosis. Mt Sinai J Med., 78(2):207-20 (2011)
  9. Kawamura K., Yao K., Shukaliak-Quandt JA , Huh J., Baig M., Quigley L., Ito N., Necker A., McFarland HF, Muraro PA, Martin R, and Ito K. Different development of MBP agonist- and antagonist-specific human TCR Tg T cells in the thymus and periphery. J. Immunology 181(8): 5462-72 (2008)
  10. Gebe JA, Unrath KA, Falk BA, Ito K., Wen L, Daniels TL, Lernmark A, and Nepom GT. Age-dependent loss of tolerance to an immunodominant epitope of glutamic acid decarboxylase in diabetic-prone RIP-B7/DR4 mice. Clin. Immunol.,121: 294-304 (2006)
  11. Quandt J.A., Baig M., Yao K., Kawamura K, Huh J., Ludwin S., Bian H.J., Bryant M., Quigley L., Nagy Z., McFarland H.F., Muraro P.A., Martin R., and Ito K. Unique Phenotypic Clinical and Pathological Features in HLA-DRB1*0401-restricted MBP111-129-specific Humanized TCR Tg mice. J. Exp. Med., 200: 223-234 (2004)
  12. Huh J., K. Yao, L. Quigley, McFarland., H.F. Muraro, P.A.. Martin, R., and Ito K. Limited repertoire of HLA-DRB1*0401-restricted MBP111-129 specific T cells in HLA-DRB1*0401 Tg mice and their pathogenic potential. J. Neuroimmunol., 151: 94-102 (2004)